Modulation of insulin-dependent diabetes mellitus (IDDM) in NOD mice by autoreactive T cells

Insulin-dependent diabetes mellitus (IDDM) is a T-cell-mediated autoimmune disease characterized by the destruction of insulin-producing beta cells in the islet of Langerhans. Islet autoantigen-specific T cells play a major role in the pathogenesis of the disease. Susceptibility loci for autoimmune diabetes such as the major histocompatability complex (MHC) may function by producing different repertoires of T cells, which could gain autoreactivity following activation, resulting in autoimmune disease. However, all the T cells infiltrating the islets are not destructive. A number of autoreactive T-cell lines capable of preventing development of IDDM have been isolated. Most of these cell lines are reactive to self I-Ag7. Presence of these regulatory T cells along with the effector cells in nonobese diabetic (NOD) mice suggests that IDDM may be a result of the imbalance of these two types of cells. Modulation of the immune response by inducing autoreactive regulatory T cells could be a way of treating autoimmune disorders.